| Project/Area Number |
07671783
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | NARA MEDICAL UNIVERSITY |
|---|
Principal Investigator |
YAMASAKI Mineo NARA MEDICAL UNIVERSITY,OBSTET.& GYNECOL., LECTURER, 医学部, 講師 (00220301)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MORIKAWA Hajime NARA MEDICAL UNIVERSITY,OBSTET.& GYNECOL., PROFESSOR, 医学部, 教授 (30030894)
|
|---|
| Project Period (FY) |
1995 – 1996
|
| Project Status |
Completed (Fiscal Year 1996)
|
| Budget Amount *help |
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1996: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
|
|---|
| Keywords | nitric oxide / preeclampsia / lipid metabolism / placenta / vascular endothelial cell / nitric oxide synthase / lipid peroxide / Western blot / ウエスタンブロット / m RNA / 妊娠 / 脂質代謝 |
|---|
| Research Abstract |
As nitric oxide (NO) is a potent vasodilator, demised production of the molecule may be involved in the pathophysiology of preeclampsia. In this study mechanism for impaired vascular endothelial cells, which has been expected to be a major factor of the decrement of the NO production, was clarified from the aspects of lipid metabolism. Compared with normal pregnant women, severe preeclamptic subjects showed higher atherogenic index, increased serum levels of serum triglycerides and lipidperoxides, lower concentrations of serum HDL-cholesterol and vitamin E and decreased ratio of polyunsaturated free fatty acid (PUFA) / saturated free fatty acid and w-3 / w-6 series of PUFA.In vitro study also supported some of the changes augment the cultured endothelial cell damage. These data suggests that severe eclamptic patients have circumstances which causes endothelial cell impairment and insufficient production of NO.We also evaluated urinary NO metabolites (NOx) in normal and preeclamptic wom
… More
en. In normal pregnancy, there was a tendency of increasing urinary NOx along the course of pregnancy and a decrease in puerperal period. On the other hand, urinary NOx in preeclampsia was significantly lower than that in normal pregnancy in correspondent gestational age. It is suggested that normal pregnancy is accompanied with increased production of NO from non-pregnant state, while preeclamptic patients is complicated by impaired production of NO compared with normal pregnancy. Studies on NO synthase (NOS) in placenta were next matter. With western blot analysis, endothelial NOS expression was detected in both of normal pregnancy and preeclampsia ; the imaging intensities in the latter group being significantly lower than those in the former group. Immunohistochemical localization of endothelial NOS in placenta from preeclampsia was noted in syncytiotrophoblast as in normal pregnancy. However, there were no difference in expression of mRNA of the enzyme between the two groups. Northern blot analysis for mRNA of neuronal NOS revealed only slight expression in the both group placenta, while protein expression assessed by western blot was not detected in any of the placenta. There were no expression of either of protein or mRNA of inducible nos in any of the placenta. These data suggested that a relative deficiency in production of nitric oxide due to decreased activity of placental endothelial NOS may contribute to the pathogenesis of preeclampsia. Less
|
